User:JoeGabriell/Bruxism

Summary (Treatment)

Buspirone, l-dopa, bromocriptine, metoclopramide, Tiagabine, Gabapentin , Tandospirone , Clodine and propranolol have evidence of efficacy in bruxism.

Summary (Pathology)

-mCPP and other 5-HT2C agonists induce oral movements and hyperkinetic oral dyskinesia through the 5-HT2C receptor in the subthalamic nucleus. -NMDA antagonists increase locomotor behavior, NRIs and alpha-2 agonists attenuate their effects, and alpha-2 antagonists potentiate their effects. -D1 agonists produce vacuous chewing movements. -Estradiol can contribute to lingual dyskinesia but also attenuates apomorphine-induced stereotypy in male rats. -Decreased membrane phosphatidylcholine turnover is implicated in dyskinesia. -SSRIs seem to desensitize 5-HT2C receptors. -5-HT2A/2C antagonist treatment antagonizes D1 agonist-induced vacuous chewing movements, increases locomotion, and enhances the efficacy of DA replacement in rodent models of Parkinson's. -Cannabinoid antagonists increase motor behavior stimulated by DA agonists. -Low doses of cannabinoid agonists decrease motor activity, whereas higher doses increase motor activity. -6-OHDA treatment in neonatal rats produces 5-HT and D1 supersensitivity during while time 5-HT antagonists attenuate D1 agonist-induced vacuous chewing movements. When given haloperidol, these rats show a doubled rate of vacuous chewing movements that persists after discontinuation and is responsive only to 5-HT2 antagonists and not D1 antagonists.

Bruxism

-Buspirone reversed SSRI-induced bruxism. (PMIDs: 10665633, 8270587, 8913405, 19740153) -l-dopa attenuates sleep bruxism. -Bromocriptine may either have no effect or may slightly improve symptoms in sleep bruxism. (, 9294496) -Diurnal/nocturnal bruxism may be characterized by hypoperfusion of the left frontal lobe, poor response to l-dopa and bromocriptine, and favorable response to metoclopramide. Hypersensitive presynaptic DA receptors are implicated. -Microcurrent electrical nerve stimulation and/or TENS may be useful in reducing pain from bruxism. -Neuroleptic-induced nocturnal bruxism (alongside akathisia) may respond to propranolol. -SSRIs cause bruxism and extrapyramidal symptoms in some. (PMIDs: 10665633, 8270587, 9640489, 8913405) -Children with ADHD taking stimulants are more likely to be affected by bruxism than children not taking stimulants. -In humans, striatal D2 BP did not differ between controls and bruxism patients, but bruxism patients showed higher side-to-side differences in D2 BP. -Sleep bruxism is associated with excessive excitability of central jaw motor pathways, and the authors note this is likely due to impaired modulation by inhibitory circuits in subcortical structures. -Sleep bruxism episodes occur during "micro-arousals", periods of increased CNS and cardiac activity. -Awake bruxism, at least in geriatric populations with pre-existing neurological pathology, seems associated with frontal lobe dysfunction. -Bruxers increased inorganic phosphate levels while chewing less than control subjects, and bruxing subjects had a lower concentration of total phosphate and phosphocreatine than nonbruxing subjects at rest. -After application of occlusional disharmony in rats for 14 days, an imbalance in striatal DOPA accumulation was noted. -Sleep bruxism is associated with higher levels of urinary catecholamines. -Long-term use of l-dopa is known to cause bruxism. -Long-term use of neuroleptics causes waking bruxism. -There may be two kinds of bruxism -- one that is idiopathic and responds to DA agonist therapy, and a nother resulting from long-term DAergic medication application. 

Epidemiology

-Bruxism is associated with anxiety, stress sensitivity, and depression, at least in awake bruxers. -Sleep bruxism is seen in 8% of the adult population, but rhythmic masticatory muscle activity of a lesser magnitude is seen in 60% of normal individuals. -Obstructive sleep apnea, loud snoring, heavy drinking, daytime sleepines, caffeine drinking, smoking, a stressful life style, and anxiety are all associated with high rates of bruxism. -Sleep bruxism is associated with feeling stressed in daily life and having poor coping strategies. -Weekly bruxers are 2.5x as likely to report smoking than never bruxers. The use of smokeless tobacco is also an independent risk factor for bruxism. -The occurrence of bruxism is associated with sleep problems. -Awake bruxism is predicted by sleep bruxism and the gagging assessment scale. Sleep bruxism is predicted by awake bruxism and the same gagging assessment scale. -Bruxism may be associated with allergies. (, 6928084) -Women show greater frequency of neuroleptic-induced extrapyramidal symptoms compared to men. -Tardive dyskinesia is more common in postmenopausal women than in men of the same age, implicating estrogen as a potentially protective factor. -Low levels of EFAs have been reported in plasma of individuals with tardive dyskinesia. -Genetically deficient CYP2D6 function has been associated with risk of developing Parkinson's disease and possibly with higher rates of EPS and akathisia. -Levetiracetam has anti-dyskinetic activity against l-dopa-induced dyskinesia in MPTP-lesioned monkeys and also potentiates the anti-dyskinetic effects of amantadine. (, 15949966, 15954135) -Bruxism linked to sleep apnea: Link -Bruxism has been linked to acid reflux  Apparently the reflux can come up high enough to irritate some nerves and muscles that control jaw function and trigger bruxism. -There's also a dry mouth-reflux-bruxism correlation I've personally noticed... especially if you're taking drugs that cause dry mouth. There's things like biotene that lubricate your mouth. I have also treated the dry mouth with using 'Breathe Right' strips on my nose to open the breathing passages a bit more so I can easily breath through my nose and not have to mouth breathe. This also helps reflux because if you have a dry mouth you don't have any saliva to keep the reflux down. -Bruxism is indicated as a cause of migraines

Drugs That Exacerbate Bruxism

-SSRIs. Though I love them dearly, they are just brutal when it comes to bruxism. -Caffeine. In my experience, caffeine in the morning isn't a problem, but afternoon caffeine is pretty rough. -Curcumin. Sad, but true; seems pretty rough on bruxism at just about any dose. -Alpha-1 Antagonists. No experience here, but the research is clear that these should worsen orofacial dyskinesia in murine models. -Nicotine. Research and anecdotal agree, nicotine does not play nice with bruxism. -Choline Precusors. (This includes CDP-choline, choline citrate, etc.) There's a good mechanism for why these drugs would worsen bruxism, and in my experience they have very profound effects in worsening the condition. -Acetycholinesterase Inhibitors. See above. -ALCAR. No idea why -- other than by means of a cholinomimetic effect -- but this stuff has always seemed to make bruxism worse. -Alcohol. One of the worst drugs out there for bruxism. I absolutely hate that this is the case, but it's been associated with bruxism both in my experience and in research. -Kudzu. No idea what the mechanism is here, but 5-HT2C antagonism inducing bruxism is possible. Still not sure what to make of that, as I would have partially expected the opposite.

Drugs That Might Exacerbate Bruxism

-Bupropion. No experience, but there are case reports of it inducing bruxism. -Amphetamine. Again, case reports of it inducing bruxism at high doses, but I've never been able to establish a clear connection between amphetamine and bruxism at therapeutic doses. -St. John's Wort. Case reports and anecdotal reports of it worsening bruxism. In my experience, Perika and SC27 absolutely did worsen bruxism, but Kira may have actually helped. -Fish Oil. Again, can't think of a mechanism to save my life, but this stuff -- at least at higher doses -- seems to cause bruxism to flare up. -NAC. Only tried it once, but I'd swear it made everything much worse. Can't think of a good mechanism for why, however.

Drugs That Might Improve Bruxism

-Memantine. I have yet to try it for this purpose, though I am increasingly eager, but there is very limited evidence to suggest that NMDA antagonists may be able to essentially eliminate bruxism. On the other hand, there's also a conceivable mechanism by which they might dramatically worsen bruxism. -St. John's Wort. As alluded to above, Kira seemed to make my bruxism better, in contrast to other SJW preparations. Kira is known to have some NMDA antagonist-like effects, so this may in part explain my experience. -Mirtazapine. Hasn't been researched for this purpose, but if the 5-HT2 antagonism of the TCAs partly explains their efficacy, then mirtazapine may be efficacious as well. Note that indirect alpha1 agonism may also have benefits. -Piracetam. Has shown efficacy in trials with dyskinesia, but that doesn't mean much. Possibly helped when I used it, but effect size was so small it might have been placebo. -Gabapentin -Deprenyl. Several anecdotal reports on the internet suggest it might show some efficacy, but seemed to worsen my bruxism when I tried it. Also not a very fun drug to take long-term. -Pantothenic Acid. One study -- IIRC -- suggested it might have some utility, and it's recommended by some anecdotally, but there's not much evidence. Can't say I've noticed much from it, but I can't discount a minor effect. -Taurine. Very small effect, but seemed to attenuate bruxism in the short-term. May have made things worse in the long-term, however. -Melatonin. Some studies to suggest it's effective in dyskinesia, but again that doesn't mean much. In my experience, it may have a small effect on bruxism, but it's by no means dramatic. -Rhodiola rosea. Anecdotally one of the best things I've tried. However, tolerance is built up very quickly

Drugs That Improve Bruxism

-Buspirone. This works well for eliminating SSRI-induced bruxism. -Clonidine. Shows excellent efficacy in clinical trials. The side effect profile is awful, though, and it carries a significant risk of depression when used long-term. -Guanfacine. Same deal as clonidine, though with fewer side effects. Still caused very substantial depressive behavior in me after several weeks of use. -Metoclopramide. This is a D2 antagonist, used at a low dose. One very important study showed efficacy, but I have a lot of hesitation regarding the long-term safety of this drug. In particular, the expectation -- as I understand it -- would be that stopping the drug would result in a horrific resurgence of bruxism. -Magnesium. Mechanism is not clear, though may be related to NMDA. This is one of the only well-proven compounds in bruxism, but it's not nearly enough for those of us with severe bruxism. Note that the oxide salt should be avoided. -Cyclobenzaprine. A muscle relaxant that is used heavily for bruxism in clinical practice. Not entirely clear if the drug is more similar amitriptyline or to cyproheptadine, but it's definitely effective in bruxism. Side effect profile can be quite brutal, however. -Nortriptyline. (Other TCAs seem to work as well.) Also attenuates bruxism, likely in part due to anticholinergic effects. Effective, used in some research, but again a nasty side effect profile. -Propranolol. There is limited research and a decent number of anecdotal reports pointing to its efficacy. -Benzodiazepines. They seem to fix bruxism instantly. If only they were suitable to long-term use. -Muscle relaxant medications may help. Nonsteroidal anti-inflammatory medications (NSAIDS) help reduce inflammation in the jaw stemming from arthritis or other causes of inflammation. -Botox

Alternative treatments

Biofeedback Link, Massaging and stretching the various muscles that may be involved in creating tension in the jaw: www.youtube.com/watch?v=1O8ArvMOzqQ Link], www.nismat.org/ptcor/tmj Link], postural treatments (Chiropractic), voice training, acupuncture, stress management, mouth guards, etc.